Piperine, an active alkaloidal constituent of the extract obtained from Piper longum and Piper nigrum, was evaluated for its antihepatotoxic potential in order to validate its use in traditional therapeutic formulations. This plant principle exerted a significant protection against tert-butyl hydroperoxide and carbon tetrachloride hepatotoxicity by reducing both in vitro and in vivo lipid peroxidation, enzymatic leakage of GPT and AP, and by preventing the depletion of GSH and total thiols in the intoxicated mice. Silymarin, a known hepatoprotective drug was tested simultaneously for comparison. Piperine showed a lower hepatoprotective potency than silymarin.
In the present study, chlorogenic acid (CGA) isolated from Anfhocephalus cadamba was screened for hepatoprotective activity by in uifro and in uiuo assay methods using carbon tetrachloride (CCI,) as a model of liver iqjury. Intraperitoneal administration of CGA to mice at a dose of 100 mgkg body weight for 8 days caused significant reversal in lipid peroxidation, enzymatic leakage, cytochrome P450 (Cyt P450) inactivation and produced enhancement of cellular antioxidant defence in CC4-intoxicated mice, revealii that the antioxidative action of CGA is responsible for its liver protective activity. CGA exhibited a better therapeutic protective action than silymarin (SM), in CCl.,-administered mice.
In view of the antioxidant properties of ascorbic acid (AA), effects of inadequate and excessive doses of AA on hepatic and pulmonary antioxidant enzymes and NADPH-dependent lipid peroxidation were investigated in the present study. Male guinea pigs, dosed daily with 0.2 mg AA/100 g b wt (inadequate) or 50 mg AA/100 g b wt (excessive) for 8 weeks, demonstrated no difference in body growth, liver and lung weights, and post-10,000 X g supernatant protein contents as compared with the control group, which was daily fed with 2 mg AA/ 100 g b wt. Inadequacy of AA decreased the hepatic and pulmonary contents of catalase, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), but it significantly increased glutathione reductase (GR) activity (p <0.005) in lung. However, levels of hepatic and pulmonary NADPH-dependent lipid peroxidation remained unaltered when the supply of AA was inadequate. Excessive doses of AA did not influence any pulmonary antioxidant enzyme, level of NADPHdependent lipid peroxidation and content of reduced glutathione (GSH), but increased the hepatic GSH-Px and GR activities. Hepatic SOD activity showed a significant decrease (p <0.01), whereas NADPHdependent lipid peroxidation and GSH contents remained unchanged. It appears that the changes in antioxidant enzymes may be a nonspecific response to AA or these changes may not be sufficient to bring about any shift in the levels of NADPH-dependent lipid peroxidation in the presence of unaltered GSH contents or other biomolecules which may act as antioxidants or free radical scavengers in the cell system.
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